Mice lacking brain-type creatine kinase activity show defective thermoregulation

Página do item simplificado
dc.contributor.authorStreijger F.
dc.contributor.authorPluk H.
dc.contributor.authorOerlemans F.
dc.contributor.authorBeckers G.
dc.contributor.authorBianco A.C.
dc.contributor.authorRibeiro M.O.
dc.contributor.authorWieringa B.
dc.contributor.authorVan der Zee C.E.E.M.
dc.date.accessioned2024-03-13T01:34:58Z
dc.date.available2024-03-13T01:34:58Z
dc.date.issued2009
dc.description.abstractThe cytosolic brain-type creatine kinase and mitochondrial ubiquitous creatine kinase (CK-B and UbCKmit) are expressed during the prepubescent and adult period of mammalian life. These creatine kinase (CK) isoforms are present in neural cell types throughout the central and peripheral nervous system and in smooth muscle containing tissues, where they have an important role in cellular energy homeostasis. Here, we report on the coupling of CK activity to body temperature rhythm and adaptive thermoregulation in mice. With both brain-type CK isoforms being absent, the body temperature reproducibly drops ~ 1.0 °C below normal during every morning (inactive) period in the daily cycle. Facultative non-shivering thermogenesis is also impaired, since CK- -/- - mice develop severe hypothermia during 24 h cold exposure. A relationship with fat metabolism was suggested because comparison of CK- -/- - mice with wildtype controls revealed decreased weight gain associated with less white and brown fat accumulation and smaller brown adipocytes. Also, circulating levels of glucose, triglycerides and leptin are reduced. Extensive physiological testing and uncoupling protein1 analysis showed, however, that the thermogenic problems are not due to abnormal responsiveness of brown adipocytes, since noradrenaline infusion produced a normal increase of body temperature. Moreover, we demonstrate that the cyclic drop in morning temperature is also not related to altered rhythmicity with reduced locomotion, diminished food intake or increased torpor sensitivity. Although several integral functions appear altered when CK is absent in the brain, combined findings point into the direction of inefficient neuronal transmission as the dominant factor in the thermoregulatory defect. © 2009 Elsevier Inc.
dc.description.firstpage76
dc.description.issuenumber1
dc.description.lastpage86
dc.description.volume97
dc.identifier.doi10.1016/j.physbeh.2009.02.003
dc.identifier.issn0031-9384
dc.identifier.urihttps://dspace.mackenzie.br/handle/10899/37376
dc.relation.ispartofPhysiology and Behavior
dc.rightsAcesso Restrito
dc.subject.otherlanguageBrown adipose tissue
dc.subject.otherlanguageCreatine kinase
dc.subject.otherlanguageCreatine kinase double knockout mice
dc.subject.otherlanguageThermogenic activity
dc.subject.otherlanguageUCP1 mRNA
dc.subject.otherlanguageWhite adipose tissue
dc.titleMice lacking brain-type creatine kinase activity show defective thermoregulation
dc.typeArtigo
local.scopus.citations34
local.scopus.eid2-s2.0-62749117195
local.scopus.updated2024-05-01
local.scopus.urlhttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=62749117195&origin=inward
Arquivos
Coleções
Artigos de periódico